Study Shows the Gut is Key in Protecting the Brain
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Posted On: 04/08/2025 5:19:15 PM
Study Shows the Gut is Key in Protecting the Brain After Stroke
Many patients who have had a stroke often suffer secondary brain damage as a result of the inflammation that is triggered during the stroke. Scientists have been working to find ways to forestall this secondary brain damage and a recent preclinical study conducted by a team at UTHealth Houston could provide a viable way to address neuroinflammation after stroke episodes.
For their study, the team focused on molecules whose role is to bind to particular receptors. These molecules are called ligands, mainly produced in the gut. Ligands are vital in facilitating cell function and signaling between different parts of the body. Some ligands are neurotransmitters and facilitate neuronal activity.
Of special interest to the researchers were AHR ligands, or aryl hydrocarbon receptor ligands. These ligands impact inflammation and immune response within brain and the entire body. After someone suffers a stroke, their gut microbiota gets compromised. This dysbiosis (imbalance) causes the AHR ligands produced within the gut to reduce.
The dysbiosis compromising AHR production also causes another type of ligand to be produced in excess outside the gut. This ligand, called Kynurenine AHR ligand, becomes overactive and throws the neuroinflammation management system into imbalance. Without sufficient AHR ligands produced inside the gut to limit the activity of Kyn AHR ligands, inflammation spikes within the brain and triggers secondary brain damage and injury.
This shows how vital gut microbiota is in reducing and regulating inflammation within the brain. It illustrates how strong the connection between one’s gut and brain is, especially after a stroke.
The UTHealth Houston research revealed that after a stroke, gut bacteria changes trigger reductions in helpful substances while allowing harmful substances to increase. This suggests that post-stroke inflammation could be averted by quickly restoring the beneficial/helpful substances in the gut.
In a previous study, the team had demonstrated how neurodegenerative diseases and stroke compromise gut microbiota, resulting in brain function problems. They also showed that dysbiosis escalated as one grew older.
Their latest research shows that restoring balance within the gut after a patient suffers a stroke can make it possible for fermentation to happen and enable ligand production to happen in ways that can reduce inflammation within the brain after a stroke.
This opens the door to new treatment approaches that focus on optimizing the connection between the brain and the gut so that post-stroke recovery happens quickly and brain damage is minimized.
For companies like Soligenix Inc. (NASDAQ: SNGX) that are investing heavily in developing new inflammation therapies, the UTHealth Houston study could provide valuable insights that may enrich R&D efforts.
Please see full terms of use and disclaimers on the BioMedWire website applicable to all content provided by BMW, wherever published or re-published: http://BMW.fm/Disclaimer
Many patients who have had a stroke often suffer secondary brain damage as a result of the inflammation that is triggered during the stroke. Scientists have been working to find ways to forestall this secondary brain damage and a recent preclinical study conducted by a team at UTHealth Houston could provide a viable way to address neuroinflammation after stroke episodes.
For their study, the team focused on molecules whose role is to bind to particular receptors. These molecules are called ligands, mainly produced in the gut. Ligands are vital in facilitating cell function and signaling between different parts of the body. Some ligands are neurotransmitters and facilitate neuronal activity.
Of special interest to the researchers were AHR ligands, or aryl hydrocarbon receptor ligands. These ligands impact inflammation and immune response within brain and the entire body. After someone suffers a stroke, their gut microbiota gets compromised. This dysbiosis (imbalance) causes the AHR ligands produced within the gut to reduce.
The dysbiosis compromising AHR production also causes another type of ligand to be produced in excess outside the gut. This ligand, called Kynurenine AHR ligand, becomes overactive and throws the neuroinflammation management system into imbalance. Without sufficient AHR ligands produced inside the gut to limit the activity of Kyn AHR ligands, inflammation spikes within the brain and triggers secondary brain damage and injury.
This shows how vital gut microbiota is in reducing and regulating inflammation within the brain. It illustrates how strong the connection between one’s gut and brain is, especially after a stroke.
The UTHealth Houston research revealed that after a stroke, gut bacteria changes trigger reductions in helpful substances while allowing harmful substances to increase. This suggests that post-stroke inflammation could be averted by quickly restoring the beneficial/helpful substances in the gut.
In a previous study, the team had demonstrated how neurodegenerative diseases and stroke compromise gut microbiota, resulting in brain function problems. They also showed that dysbiosis escalated as one grew older.
Their latest research shows that restoring balance within the gut after a patient suffers a stroke can make it possible for fermentation to happen and enable ligand production to happen in ways that can reduce inflammation within the brain after a stroke.
This opens the door to new treatment approaches that focus on optimizing the connection between the brain and the gut so that post-stroke recovery happens quickly and brain damage is minimized.
For companies like Soligenix Inc. (NASDAQ: SNGX) that are investing heavily in developing new inflammation therapies, the UTHealth Houston study could provide valuable insights that may enrich R&D efforts.
Please see full terms of use and disclaimers on the BioMedWire website applicable to all content provided by BMW, wherever published or re-published: http://BMW.fm/Disclaimer
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